Background and Purpose- Depression after stroke is common. Like stroke, transient ischemic attack (TIA) is a manifestation of long-term atherosclerotic damage to the brain. However, the risk of depression developing after a TIA is uncertain. We studied whether TIA increases the risk of incident late-life depression. Methods- A cohort study of 5095 inhabitants of Rotterdam, the Netherlands, was performed between 1993 and 2005. Participants were aged 56 years or older and free of depression at baseline. TIA and depression were identified through regular standardized examinations and continuous monitoring of medical records. We estimated hazard ratios (HR) with time-varying Cox regression analyses, adjusting for sociodemographic and health-related factors. Results- During follow-up, 407 depressive syndromes occurred, of which 103 met criteria of the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM) for depressive disorders. TIA was significantly associated with the risk of incident depressive syndromes (HR, 1.68; 95% CI, 1.12-2.51) and DSM-defined depressive disorders (HR, 2.42; 95% CI, 1.26-4.67). The risk of depressive syndromes increased with the number of TIA a person had experienced (HR, 1.45; 95% CI, 1.17-1.81), as did the risk of depressive disorders (HR, 1.63; 95% CI, 1.18-2.24). In persons without a history of depression at baseline, we found an almost 3-fold increased risk of DSM-defined depressive disorders (HR, 2.91; 95% CI, 0.96-8.81). Conclusions- TIA was independently associated with an increased risk of incident depression. Our finding suggests that symptomatic cerebrovascular disease increases the vulnerability to late-life depression. Copyright

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Keywords cohort study, depression, transient ischemic attack
Persistent URL dx.doi.org/10.1161/STROKEAHA.110.604405, hdl.handle.net/1765/33377
Citation
Luijendijk, H.J., Stricker, B.H.Ch., Wieberdink, R.G., Koudstaal, P.J., Hofman, A., Breteler, M.M.B., & Tiemeier, H.W.. (2011). Transient ischemic attack and incident depression. Stroke, 42(7), 1857–1861. doi:10.1161/STROKEAHA.110.604405